Micro 410 Set 2 Parsek

Front 1

In what form do cyanobacterial heterocysts feed Nitrogen to vegetative cells?

Back 1

glutamine.

Front 2

What exchange occurs between heterocysts and vegetative cells in filamentous cyanobacteria?

Back 2

Vegetative cell gives: glutamate, e- donor for Photosystem I ATP synthesis

Heterocyst gives: glutamine

Front 3

What two enzyme systems do heterocysts use to assimilate atmospheric N2?

Back 3

Glutamine Synthetase/GOGAT
glu + NH3 --(GS)--> gln
gln + a-ketoglutarate --(GOGAT)--> 2 glu

Glutamate Dehydrogenase
a-ketoglutarate --> glu

Front 4

How do bacteroids feed nitrogen to the host plant?

Back 4

gln
asn

Front 5

What exchange occurs between bacteroids and host plants?

Back 5

Plant gives: TCA Cycle intermediates, sugars, organic acids

Bacteroid gives: gln, asn

Front 6

What do bacteroids do with TCA cycle intermediates from the plant?

Back 6

Run TCA Cycle --> Generate reducing power for ETChain --> ATP

Front 7

What triggers the A Signal in myxobacteria and what does it do?

Back 7

C/N/P Starvation --> ppGpp made --> A signal released (small peptides)

A signal functions as a quorum sensor. Once critical concentration is reached SasR initiates transcription of FruA.

Front 8

What is the function of C Signaling?

Back 8

Coordinates cell movement and aggregation, triggers phosphorylation of FruA

FruA-P --> aggregation, streaming, myxospore formation

Front 9

Describe the mechanism involved in myxobacterial social motility.

Back 9

Used by rafts of 15-20 cells traveling in a wave.

Type IV Pili: 2 ATP Driven motors
PilB - extends pilus by adding pilin units to base
PilT - retracts pilus by removing pilin units from base.

Works like grappling hook: reel self forward

Front 10

Describe the mechanism involved in myxobacterial adventurous motility.

Back 10

Secretion of "slime jets"

or cytoskeletal proteins may adhere to the surface and be used to corkscrew the cell forward across the medium.

Front 11

What is the function of Nod factors?

Back 11

Secreted by Rhizobial cells to encourage curling of root hair + increased plant cell division --> nodule formation

Front 12

What class of compounds do root hairs secrete to attract Rhizobial cells?

Back 12

Flavonoids.

Can attract/deter: produce selectively to direct infection to specific areas of plant.

Front 13

What helps to ensure host plant/Rhizobial species specificity?

Back 13

Ca-Binding Proteins: binds Ca on root tip
Lectins: adhere to specific polysaccharides on root hair.
Flavonoids: plant flavonoids will only attract certain Rhizobial cells.

Front 14

What is homologous recombination?

Back 14

Exchange of homologous regions of ssDNA on 2 DNA molecules --> heteroduplex

Next round of replication --> 2 different genomes:
1. original genome
2. strand of DNA that has the exchanged part in it

Front 15

What is nonhomologous recombination?

Back 15

Exchange of nonhomologous or unevenly sized regions of ssDNA --> 1 genome with gene deletions, 1 genome with gene duplications.

May also put incorrect gene under control of wrong promoter.

Front 16

What base does 5-Bromouracil substitte for?

Back 16

Subs for Thymine but pairs with Guanine, not Adenine

A/T --> 5-Br Uracil/G --> C/G Base pair

Front 17

What is the most damaging effect of ionizing radiation?

Back 17

Breaks P-O-P DNA backbone --> may linearize chromosome.

Creates AP sites by detaching bases

Front 18

What is the difference between Insertion Sequences and Transposons?

Back 18

Length and Genetic content

IS = smaller, 800-2000bp, only transposase gene

Tn = larger >2000bp, caries transposase + other genes (ex. antibiotic resistance), flanked by IS on either side.

Both flanked by palindromic sequences.

Front 19

What are the two modes of transposition?

Back 19

Replicative: Tn/IS replicates self and inserts copy in new location.

Nonreplicative: "cut and paste" IS/Tn excises and reinserts self elsewhere.

Front 20

Why are IS/Tn's problematic?

Back 20

They can insert themselves in the middle of a gene --> interrupt gene --> nonfunctional protein

Front 21

What is a nonsense mutation?

Back 21

Change that results in a STOP codon --> early termination of peptide synthesis

Severity of effect depends on where peptide got truncated

Front 22

What is a missense mutation?

Back 22

Switch in 1st or 2nd letter of codon --> different/wrong AA inserted

Front 23

What is a frame shift mutation?

Back 23

Deletion/Insertion of bases in a number that is NOT a multiple of 3

--> reading frame shift. every codon downstream of mutation is ruined

necessarily fatal for the peptide.

Front 24

What is light repair and what does it fix?

Back 24

Repairs thymine dimers due to UV light

Photolyase enzyme: uses light E to break thymine dimers apart.

Front 25

What is Damaged Base Repair and what does it fix?

Back 25

repairs modified bases.

-Enzyme detaches base from ribose --> AP site
-AP endonucleases excise portion of DNA surrounding AP site
-DNA Pol I + Ligase repair.

Front 26

What is Dark/Nucleotide Excision repair and what does it fix?

Back 26

Fix: damaged regions of DNA

UrvABC protein complex
-Nicks DNA 8bp 5' of damage, 4-5bp 3' of damage
-Helicase unwinds + removes damaged region
-DNA Pol I + Ligase repair.

Front 27

What is Recombinational/Post-replication Repair and what does it fix?

Back 27

Fixes when DNA Pol III had to skip replicating a damaged region of DNA --> region of damaged ssDNA remains on chromosome

-RecA protein excises homologous ssDNA from new sister chromosome
-RecA and Ligase insert borrowed strand into damaged unreplicated chromosome for DNA Pol to use as template.

Front 28

How does the Methyl Directed Mismatch Repair system work?

Back 28

Dictates which base is wrong in a mismatched bp.

-MutS: looks for + binds damaged DNA
-MutH: binds nearest -CH3 grp to MutS
-MutL: binds MutS + MutH, uses ATP to nick nonmethylated strand
-ssDNA exonuclease cuts out damaged region
-DNA Pol I/Ligase repair.

Front 29

What is SOS repair and what does it fix?

Back 29

SOS repair = last ditch effort when all other repair mechanisms are saturated.

-LexA protein represses repair enzyme operons and error prone DNA Pol operons.
-RecA protein: Inactivates LexA repressor --> increased repair enzyme expression BUT also increased error prone DNA Pol IV + V.

Front 30

What is the average spontaneous mutation rate in bacterial genes?

Back 30

~1 mutation per 1,000,000 cell divisions

~10^-6

Front 31

What is one advantage of a high mutation rate (as in mutator strains)?

Back 31

Allows bacteria a better chance to adapt to a quickly changing environment. Higher SMR --> more mutations --> more chances for a favorable adaptation.

Front 32

In MCP-directed chemotaxis, what happens upon addition of an attractant?

Back 32

Attractant binds Chemosensor (binding protein)

Sensor/Attractant binds MCP

MCP --> conf. change that allows methylation

CheR methylates slowly.

Front 33

Why is the adaptation period slow and transient?

Back 33

CheR methylates MCP II slowly.

Transient because once appropriate level of methylation is reached or levels of attractant become stable, CheR stops methylating.

Cell resumes unbiased random run/tumble frequency until environment changes.

Front 34

Why is the chemotactic de-adaptation period so much shorter than the adaptation period?

Back 34

CheB, which de-methylates MCP II, acts much more quickly than CheR did.

Front 35

How do cells involved in chemotaxis compare their past and present environments?

Back 35

Compare the level of association of MCP II with attractant/binding protein to level of MCP II methylation.

Assoc. w/binding protein is instantaneous and reflects present environment; methylation is slow and reflects past.

Front 36

When does CheA autophosphorylate itself?

Back 36

In the presence of unfavorable environmental conditions: no attractant or presence of repellent.

CheA-P transfers P to CheY so it can trigger CW flagellar rotation --> cell tumbles.

Front 37

How does the Phosphotransferase System regulate chemotaxis?

Back 37

Levels of phosphorylation of Enzyme I measure concentration of PTS substrate.

High substrate --> low Enzyme I-P levels inhibit CheA.

Less CheA-P --> Less CheY-P --> Less CW rotation/tumbles; cell has longer runs.

Front 38

Which Che proteins are involved in termination of chemotactic response?

Back 38

CheA-P --> phosphorylate CheB and CheY
CheB-P --> de-methylate MCP II
CheY-P --> CW flagellar rotation (tumble)

Front 39

Why is liver extract added to chemicals being subjected to the Ames test?

Back 39

Liver makes mixed function oxygenases which often convert chemicals in to mutagens or carcinogens.

Front 40

What is the basis of the Ames test for mutagen/carcinogenicity?

Back 40

Growth of a supposedly auxotrophic mutant indicates mutation back into prototrophs.

More mutations = more prototrophs = more growth.

So level of growth is proportional to mutagenicity of compound in question.